Background: Available hyaluronic acid dermal fillers have unique biophysical properties that influence their clinical utility, longevity, and aesthetic outcomes.
Objective: To evaluate the effectiveness and durability of a cohesive polydensified matrix hyaluronic acid dermal filler (CPM-HA) for the treatment of etched-in fine facial lines.
Materials And Methods: Subjects with etched-in fine lines of the forehead, cutaneous lip, melolabial folds, nasolabial folds, and/or radial cheek received treatment with CPM-HA mixed with lidocaine and epinephrine, with an optional touch-up treatment at Week 2, if deemed necessary.
The mouse Engrailed genes, En1 and En2, play an important role in the development of the cerebellum from its inception at the mid/hindbrain boundary in early embryonic development through cell type specification events and beyond. In the absence of En1, the cerebellum and caudal midbrain fail to develop normally--a phenotype that we have previously reported to be strain dependent. On the 129/S1 strain background, En1 null alleles lead to mid/hindbrain failure, whereas on the C57BL/6 background, En1 deficiency is compatible with near normal cerebellar development.
View Article and Find Full Text PDFAutism spectrum disorder (ASD) represents a major mental health problem with estimates of prevalence ranging from 1/500 to 1/2000. While generally recognized as developmental in origin, little to nothing is certain about its etiology. Currently, diagnosis is made on the basis of a variety of early developmental delays and/or regressions in behavior.
View Article and Find Full Text PDFEngrailed-1, a homeobox containing transcriptional repressor, is known to play an important role in the development of the vertebrate limb. In its absence, mouse limbs develop with improper specification of dorsal identity and digit abnormalities. We report here that specific malformations in the mutant limb are dependent on strain background.
View Article and Find Full Text PDFThe mouse homeodomain protein, Engrailed-1, is generally viewed as an essential player in the early establishment and maintenance of the midbrain/hindbrain region that gives rise to the cerebellum and midbrain. In keeping with this, engineered null mutations at this locus have been reported to lead to perinatal lethality accompanied by near-total absence of cerebellar and caudal midbrain structures. We report here that these cerebellar phenotypes are nearly completely suppressed on a C57BL/6J genetic background.
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